Metastasis is a major cause of death in patients with breast cancer. In the process of cancer development, epithelial-mesenchymal transition (EMT) is crucial to promoting the invasion and migration of tumor cells. In a previous study, the role of resveratrol in migration and metastasis was investigated in MDA-MB-231 (MDA231) human breast cancer cells and a xenograft-bearing mouse model. Additionally, the related mechanism was explored. In the present study, in vitro Transwell assays showed that resveratrol can inhibit the migration of transforming growth factor (TGF)-β1-induced MDA231 cells in a concentration-dependent manner. An enzyme-linked immunosorbent assay (ELISA) showed that resveratrol can reduce the secretion of matrix metalloproteinase (MMP)-2 and MMP-9. Immunofluorescence was performed to confirm the expression of EMT-related markers. Immunofluorescence assays confirmed that resveratrol changed the expression of the EMT-related markers E-cadherin and vimentin. Western blot analysis demonstrated that resveratrol decreased the expression levels of MMP-2, MMP-9, Fibronectin, α-SMA, P-PI3K, P-AKT, Smad2, Smad3, P-Smad2, P-Smad3, vimentin, Snail1, and Slug, as well as increased the expression levels of E-cadherin in MDA231 cells. In vivo, resveratrol inhibited lung metastasis in a mouse model bearing MDA231 human breast cancer xenografts without marked changes in body weight or liver and kidney function. These results indicate that resveratrol inhibits the migration of MDA231 cells by reversing TGF-β1-induced EMT and inhibits the lung metastasis of MDA231 human breast cancer in a xenograft-bearing mouse model.

Ganoderma lucidum extract (GLE) has shown positive effects for tumor treatment. However, the molecular mechanism of GLE treatment is unknown. In this study, a Hepa1-6-bearing C57 BL/6 mouse model was established to explore the anti-tumor and immunostimulatory activity of GLE treatment. The results showed that GLE effectively inhibited tumor growth without hepatic/renal toxicity and bone marrow suppression, and might enhancing immunological function. Based on the mRNA profiles of GLE treated and untreated mice, 302 differentially expressed (DE) mRNAs were identified and 6 kernel mRNAs were identified from the established protein-protein interaction (PPI) network. Quantitative RT-PCR and western-blot analysis indicated that 6 mRNAs have had statistically significant differences between the GLE treated and untreated mice. Furthermore, four kernel pathways were isolated from the KEGG-Target network, including the Jak-STAT signaling pathway, T cell receptor signaling pathway, PI3K-Akt signaling pathway, and cytokine-cytokine receptor interaction. Western-blot and cytokine detection results demonstrated that GLE suppressed growth and proliferation of tumors by the Jak-STAT signaling pathway, T cell receptor signaling pathway and PI3K-Akt signaling pathway, but also regulated the expression levels of serum immune cytokines and improved the anti-tumor immunostimulatory activity.